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Mitochondria pp 241–269Cite as

The Mitochondrial Permeability Transition Pore – from Molecular Mechanism to Reperfusion Injury and Cardioprotection

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Part of the book series: Advances in Biochemistry in Health and Disease ((ABHD,volume 2))

Abstract

In most cells, the primary role played by the mitochondria is the provision of ATP through oxidative phosphorylation to support the numerous energy requiring processes. This is especially so in tissues such as the beating heart where the provision of ATP to meet the demands of muscle contraction and the maintenance of ionic homeostasis are especially heavy. Indeed, even under resting conditions, the heart cannot survive on glycolytic ATP alone and rapidly ceases to beat when oxidative phosphorylation is impaired by anoxia or ischemia. It comes as something of a surprise, therefore, to discover that within the mitochondria there exists a latent mechanism that, once activated, converts them from organelles that energise the cell to those that actively kill the cell via apoptosis or necrosis. This transition, reminiscent of the fictional Dr Jeckyll who turns into the murderous Mr Hyde, is mediated within the mitochondria by the opening of a non-specific pore in the mitochondrial inner membrane, known as the mitochondrial permeability transition pore (MPTP).

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Authors
  1. Andrew P. Halestrap
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  2. Samatha J. Clarke
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  3. Igor Khalilin
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Editor information

Editors and Affiliations

  1. Department of Pharmacology, University of South Alabama, Mobile, AL, 36688-0001, USA

    Stephen W. Schaffer

  2. Bristol Royal Infirmary, Bristol, BS2 8HW, UK

    M-Saadeh Suleiman

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Halestrap, A.P., Clarke, S.J., Khalilin, I. (2007). The Mitochondrial Permeability Transition Pore – from Molecular Mechanism to Reperfusion Injury and Cardioprotection. In: Schaffer, S.W., Suleiman, MS. (eds) Mitochondria. Advances in Biochemistry in Health and Disease, vol 2. Springer, New York, NY. https://doi.org/10.1007/978-0-387-69945-5_11

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